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Biomedical subjects

F Meyer

Publications and source records attributed to F Meyer.

At least 271 records · Page 15Linked to original sources
PubMed1976

[Heart and circulatory effects of quinidine stereoisomers].

Quinidine sulfate shows dose-related activity. On the cardio-vascular system of anaesthetized cats. It reduces heart rate, prolongs QRS and QT of the ECG, lowers peripheral blood pressure and depresses slightly myocardial contractility. Quinidine hydrochloride lowers blood pressure but alters the ECG only in very high doses. Epiquinidine has no blood pressure lowering activity. According to the Easson and Stedman hypothesis this may be the result of stereoselectivity of alpha-adrenergic receptors. Only very high doses of the epimer produce a transient decrease of blood pressure. The ECG-waves are, however, markedly altered. QT is prolonged only with epiquinine-epiquinidine-sulfate. The salts of epiquinidine tested are much better water-soluble than those of quinidine.

Animals↗
PubMed1976

[Local anesthesia after percutaneous administration. I].

Local anesthesia of the intact skin is difficult because of the skin barrier to epicutaneous penetration. Using solutions of local anesthetics in organic agents, which have the ability of penetrating the skin without causing irreversible damage and enhancing the percutaneous absorption of all materials dissolved therein, topical anesthesia seems to be attainable. A satisfactory method for determining pain threshold in uninjured skin of animals has been set up. Measurments of the pricking pain threshold have been made by exposing the skin of guinea-pigs to defined mechanical and electrical stimuli. A nociceptive muscle reflex (twitch) has been taken as the index of pain sensation. The suppression of this twitch has been used as an indicator of anesthetic potency. Two methods have been applied with varying parameters: stimulation at a fixed intensity until the pain threshold was reached (duration of anesthetic effect) and stimulation with increasing stimulus strenght until the cutaneous reflex was elicited (intensity or "depth" of anesthesia). The local anesthetic effects of lidocaine, fomocaine and procaine bases were studied, after dissolving them in dimethyl sulfoxide (DMSO), a wellknown carrier for transmembranal application. The duration of local anesthesia measured by electrical stimuli was longer than that obtained with mechanical ones. Differences are discussed. All results indicate that fomocaine (5%) has a greater local anesthetic potency than procaine (5%) but both are less active than lidocaine (5%). No effect could be seen after application of DMSO alone.

Administration, Topical↗
PubMed1976

[Effects of pentaformylgitoxin (gitoformate) on the cardiovascular system of anesthetized cats].

In small and medium doses 3 beta, 14 beta-dihydroxy-16 beta-formyloxy-5 beta-card-20-[22]-enolide-3-tetraformyltridigitoxoside (pentaformylgitoxin; gitoformate) shows a greater positive inotropic and blood pressure increasing potency than do digitoxin and beta-acetyldigoxin. In high doses this influence on contractility is exceeded by digitoxin, that on blood pressure is equalled. None of the substances tested changes heart rate. Arrhythmias with gitoformate are only seen in lethal doses, with digitoxin and beta-acetyldigoxin two dose levels earlier.

Animals↗
PubMed1975

[The reciprocal actions of phenprocoumon (Marcumar) with human serum albumin, erythrocytes and blood].

The binding properties of phenprocoumon (PhC) to human serum albumin (HSA) and to red blood cells (RBC) were determined by using the equilibrium dialysis. Analysis of PhC-binding data to HSA at pH 7.4 and temperatures of 10 degrees C and 27 degrees C resulted in binding constants (k) of 11.8 - 10(4) and 7.0 - 10(4), in free standard enthalpy changes deltaG0 of -6.658 and -6.651 kcal/mol, and in standard enthalpy change TdeltaS0 of 1.386 and 1.469 kcal/mole, respectively. The standard enthalpy change deltaH0 was -5.182 kcal/mole for both temperatures. These results indicate that the binding between PhC and HSA is predominantly effected by hydrophobic interactions. At pH 7.4 the binding to HSA is essentially characeterized by two straight lines of binding, whereas at pH 9 and 10 there are three. With increasing pH more binding sites become free and the affinity of PhC to HSA grows. Studies of binding properties to RBC indicate a strong binding of PhC to hemoglobin (k 7.9 - 10(5)), but only a weak one to red cell membranes (binding ratio hemoglobin to ghosts 66 : 1). In a combined system of HSA and RBC, competition occurs between both components and therefore the strength of binding decreases. At therapeutic PhC-concentrations, 91.7% of the PhC are bound to the whole blood, 20.8% to RBC, and 70.9% to HSA. With increasing concentrations of PhC the binding to RBC declines to 10.5% accompanied by an approximately unchanged binding to whole blood of 92.1%; whereas binding to HSA increases to 81.6%. The affinity of PhC to HSA grows larger than its affinity to RBC. The total binding to blood remains unchanged within a 21-fold range and it is predominantly determined by the affinity of HSA to PhC.

Blood↗
PubMed1975

[Rodenticidal action of warfarin/4th communication: Binding to serum albumin of mice and rats (author's transl)].

The binding properties of 3-(1'-phenyl-2'-acetylethyl)-4-hydroxycoumarine (warfarin-Na) to serum albumin of mice and rats were determined by using the equilibrium dialysis. The binding percentage (beta), the binding capacity (K), and the association constant (K1) were calculated. The results are characteristic for a strong binding of warfarin to serum albumin of rats but only a small one to serum albumin of mice, caused probably by the different albumin structures of these species.

Animals↗
PubMed1975

[Action of fomocaine on heart and circulation (author's transl)].

Fomocaine shows antiarrhythmic properties. It prolongs the periods of the ECG (anaesthetized cats) and the functional refractory period (left atria of guinea-pigs, electrically driven). Effects on these parameters are qualitatively the same as with quinidine. Quantitatively fomocaine prolongs the functional refractory period in the same, the PQ-interval to a greater extent than does quinidine. In contrast quinidine has a greater effect on QRS- and QT-interval. Up to higher doses fomocaine's efficacy on contractility (dp/dtmax) and blood pressure is opposite to quinidine because they are increased by fomocaine and decreased by quinidine. The lack of toxic ECG-signs prior to lethal dosis makes fomocaine dangerous in overdosage.

Animals↗